Initial studies of reovirus by thin sectioning suggest that the virus may enter cells not only by viropexis but by direct penetration and this investigation will be continued. In addition, cell membranes will be purified by the Tris buffer method and layered on sucrose gradients. Adenovirus, reovirus and influenza virus will be adsorbed to the membranes in the cold, and after warming, will be examined by thin sectioning and negative staining to determine whether there are changes in configuration or structure of the capsomeres or spikes. In the case of influenza the virus RNA will be labeled with H3 uridine and it will be determined whether release occurs. Further study of visna virus will be undertaken, with particular emphasis on the manner in which fusion is produced. Cultures will be embedded in situ at intervals after addition of the virus in an attempt to determine whether the virus forms bridges between cells, thus initiating the fusion process. Preliminary study of herpes saimiri virus suggests that virus may differentiate in the cytoplasm as well as in the nucleus. It is proposed to separate nuclear and cytoplasmic fractions and determine whether the viral DNA and proteins differ. Whether cells enucleated with cytocalasin B permit development of this strain of herpes virus will also be investigated. Early stages in the development of vaccinia virus have been seen after release of hydroxyurea block. Apparently the nucleoprotein passes directly into the virus, where it appears to become very dense, probably as a result of coiling or folding. These studies will be extended. The neutralization of herpes simplex virus will be examined to determine whether antibody and complement cause lysis of the envelope. The effect of antibody on fusion will be also examined. The lesions produced by herpes simplex virus will be examined in the livers of mice after I.V. injection of the virus.